These results suggest that endothelial cell injury plays a significant role in the pathogenesis of PF, and that lung WR of 123I-MIBG, which is a specific marker of endothelial damage, can serve as a novel diagnostic tool to evaluate the functional severity of PF.

Background: It has been speculated that clarithromycin (CAM), a 14-membered ring macrolide, possesses antitumor effects besides antimicrobial and anti-inflammatory effects. Method: We evaluated the effects of CAM on the growth and invasiveness of A549 lung adenocarcinoma cells. Results: Although CAM did not affect the growth of A549 cells, the Matrigel invasion assay showed that the potential of invasion was diminished by CAM treatment. When analyzed by flow cytometry, CAM suppressed α₂- and β₁-integrin expression. Furthermore, thymidine phosphorylase (TP) expression was diminished by CAM treatment in a dose-dependent manner. A specific TP inhibitor also suppressed β₁-integrin expression in flow cytometric analysis. Conclusions: These results suggest that CAM may suppress invasive activity of A549 cells in part by diminishing the expression of TP, α₂- and β₁-integrin, which may be a downstream signal of the TP pathway, and that CAM could be useful in the treatment of lung adenocarcinoma.

ObjectiveApoptosis may be involved in the pathophysiology of cachexia in patients with chronic obstructive pulmonary disease (COPD). The purpose of this study is to assess the potential role of the Fas-Fas ligand (FasL) system in cachexic patients with COPD.Patients and Methods We measured the circulating levels of soluble FasL (sFasL), with a newly developed, highly sensitive enzyme-linked immunosorbent assay system in seventy patients with COPD and forty-seven control subjects.Results The levels of sFasL in the COPD patients were significantly lower than those in the control subjects (46±29 vs. 55±28 pg/ml; p<0.05), whereas the levels of soluble Fas (sFas) remained unchanged between the two groups. The significant correlation between the levels of sFasL and sFas, observed in the control subjects (r=0.304; p<0.05), was absent in the COPD patients. Cachexic COPD patients with a relatively lower BMI (BMI <20 kg/m 2 , n=45) and %fat (%fat <20%, n=34), showed significantly increased levels of sFasL compared to non-cachexic COPD patients with a relatively higher BMI (BMI 20 kg/m 2 , n=25) and %fat (%fat 20%, n=36) (BMI; 51±33 vs. 36±15 pg/ml; p<0.05. %fat; 55±33 vs. 37±21 pg/ml; p<0.01), due to the inverse relationships between the body composition measurements and the levels of sFasL observed exclusively in the patients (BMI; r=-0.307; p<0.05. %fat; r=-0.283; p<0.05).Conclusion These results may suggest that the FasFasL system does not play a significant role in the potential triggers of enhanced apoptosis leading to skeletal muscle wasting and adipose tissue depletion in cachexic patients with COPD. (Internal Medicine 44: 1137-1143, 2005)

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